Evidence map›Paper›PMID 24625974›Full record

ArticleCell death & disease2014

NK cell intrinsic regulation of MIP-1α by granzyme M.

N Baschuk, N Wang, S V Watt, H Halse, C House, P I Bird, R Strugnell, J A Trapani, M J Smyth, D M Andrews

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.9field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
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  8. Review
  9. Article
  10. Natural Killer Cells: Angels and Devils for Immunotherapy.International journal of molecular sciences · 2017
    Review
  11. Article
  12. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 1 country.

N BaschukCancer Immunology Program, Trescowthick Laboratories, Peter MacCallum Cancer Centre, St. Andrews Place, East Melbourne, Victoria 3002, Australia.
N WangDepartment of Microbiology and Immunology, The University of Melbourne, Parkville, Victoria 3010, Australia.
S V WattCancer Immunology Program, Trescowthick Laboratories, Peter MacCallum Cancer Centre, St. Andrews Place, East Melbourne, Victoria 3002, Australia.
H HalseCancer Immunology Program, Trescowthick Laboratories, Peter MacCallum Cancer Centre, St. Andrews Place, East Melbourne, Victoria 3002, Australia.
C HouseCancer Immunology Program, Trescowthick Laboratories, Peter MacCallum Cancer Centre, St. Andrews Place, East Melbourne, Victoria 3002, Australia.
P I BirdDepartment of Biochemistry and Molecular Biology, Monash University, Melbourne, Victoria 3800, Australia.
R StrugnellDepartment of Microbiology and Immunology, The University of Melbourne, Parkville, Victoria 3010, Australia.
J A Trapani1] Cancer Immunology Program, Trescowthick Laboratories, Peter MacCallum Cancer Centre, St. Andrews Place, East Melbourne, Victoria 3002, Australia [2] Department of Pathology, The University of Melbourne, Parkville, Victoria 3010, Australia [3] Sir Peter MacCallum Department of Oncology, The University of MelbourneParkville, Victoria 3010, Australia.
M J Smyth1] Cancer Immunology Program, Trescowthick Laboratories, Peter MacCallum Cancer Centre, St. Andrews Place, East Melbourne, Victoria 3002, Australia [2] Department of Pathology, The University of Melbourne, Parkville, Victoria 3010, Australia [3] Sir Peter MacCallum Department of Oncology, The University of MelbourneParkville, Victoria 3010, Australia [4] Immunology in Cancer and Infection Laboratory, Queensland Institute of Medical Research, Herston Qld 4006, Australia [5] School of Medicine, University of Queensland, Herston Qld 4006, Australia.
D M Andrews1] Cancer Immunology Program, Trescowthick Laboratories, Peter MacCallum Cancer Centre, St. Andrews Place, East Melbourne, Victoria 3002, Australia [2] Department of Pathology, The University of Melbourne, Parkville, Victoria 3010, Australia [3] Sir Peter MacCallum Department of Oncology, The University of MelbourneParkville, Victoria 3010, Australia.
Peter MacCallum Cancer Centre · AUUniversity of Melbourne · AUMonash University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Granzymes are generally recognized for their capacity to induce various pathways of perforin-dependent target cell death. Within this serine protease family, Granzyme M (GrzM) is unique owing to its preferential expression in innate effectors such as natural killer (NK) cells. During Listeria monocytogenes infection, we observed markedly reduced secretion of macrophage inflammatory protein-1 alpha (MIP-1α) in livers of GrzM-deficient mice, which resulted in significantly impaired NK cell recruitment. Direct stimulation with IL-12 and IL-15 demonstrated that GrzM was required for maximal secretion of active MIP-1α. This effect was not due to reduced protein induction but resulted from heightened intracellular accumulation of MIP-1α, with reduced release. These results demonstrate that GrzM is a critical mediator of innate immunity that can regulate chemotactic networks and has an important role in the initiation of immune responses and pathogen control.

Indexed as

Immunity, InnateAnimalsCells, CulturedChemokine CCL3Chemotaxis, LeukocyteCoculture TechniquesDisease Models, AnimalGranzymesHumansInterleukinsKiller Cells, NaturalListeria monocytogenesListeriosisMiceMice, KnockoutTime FactorsCCL3 protein, humanCcl3 protein, mouseChemokine CCL3GranzymesGzmb protein, mouseGZMM protein, humanGzmm protein, mouseInterleukins

Identifiers

PMID24625974
PMCPMC3973215
OpenAlexW1997666580

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.